Extranodal malignant non-Hodgkin lymphoma of mucosa-associated lymphoid tissue type (MALT lymphoma) represents a subtype of B-cell lymphoid malignancies with distinct clinicopathological features and is often associated with a favorable prognosis. Recent cytogenetic studies have revealed that t(11;1
Molecular-cytogenetic comparison of mucosa-associated marginal zone B-cell lymphoma and large B-cell lymphoma arising in the gastro-intestinal tract
✍ Scribed by Thomas F.E. Barth; Martin Bentz; Frank Leithäuser; Stephan Stilgenbauer; Reiner Siebert; Magdalena Schlotter; Richard F. Schlenk; Hartmut Döhner; Peter Möller
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 345 KB
- Volume
- 31
- Category
- Article
- ISSN
- 1045-2257
- DOI
- 10.1002/gcc.1150
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✦ Synopsis
Abstract
Extranodal B‐cell lymphoma of mucosa‐associated lymphoid tissue (MALT) type may represent a model of lymphoma progression, because a small cell component frequently occurs in the large cell variants. We studied 52 extranodal B‐cell lymphomas: 18 extranodal marginal zone B‐cell lymphomas of MALT type (MZBL,MT), 7 MZBL,MT of the gastro‐intestinal tract with a diffuse large B‐cell component (giMZBL__plus__LBCL), and 27 diffuse large B‐cell lymphomas of the gastro‐intestinal tract without small cell component (giLBCL). Analytical techniques were comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH). The translocation t(11;18) was found as the sole aberration in two MZBL,MT only. In contrast to this, t(11;18)‐negative MZBL,MT were characterized by frequent gains on chromosome 3 and DNA amplifications on 2p13–p15. Furthermore, we found a clonal lymphoma progression from the small to the large cell component with accumulation of gains and losses of chromosomal material in the large cell component in giMZBL__plus__LBCL. Aberrations overlapping with MZBL,MT and giMZBL__plus__LBCL included losses on chromosome 13, amplifications of the REL proto‐oncogene, or gains on chromosome 12. In addition, the large cell component revealed gains on 8q24, including amplifications of the MYC proto‐oncogene, and losses on 2q. The giLBCL had frequent gains on chromosomes 12 and 9, as well as on 11q, and losses on 6q. We conclude that, based on the distinctive and partly overlapping patterns of genetic aberrations, MALT lymphomas can be divided into different genetic subgroups. © 2001 Wiley‐Liss, Inc.
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